The purpose of this project is to define the mechanisms whereby cells of yersiniae obtain iron during growth in vivo and to examine the consequences of iron-starvation in these facultative intracellular parasites. Although the cells fail to produce detectable siderophilins (small molecular weight iron-carriers), they do excrete a compound under conditions of iron-deficiency which can be converted to a siderophilin by enteric bacteria. The nature of this compound is under study. Yersiniae rely on direct transport of hemin, probably obtained from hemopexin, during growth in vivo. The process of hemin transport is being investigated and is known to involve a surface site which also serves to absorb the bacteriocin pesticin. Using pesticin as a probe, sensitive bacteria (capable of using hemin is a source of iron) were converted to osmotically stable spheroplasts. The mechanism of this conversion is also under study. Since yersiniae need not rely on inorganic iron during growth in vivo, the cells are being used to distinguish between deleterious effects seen following its injection due to filling a nutritional role versus those caused by inhibiting normal defence mechanisms.